Anatomy - Toupet Fundoplicatio for GERD, Robot-Assisted

The stomach is a muscular hollow organ located between the esophagus and duodenum, situated in the left and central upper abdomen directly beneath the diaphragm. When moderately filled, it is 25 – 30 cm long and has a storage capacity of 1.5 liters, which can extend up to 2.5 liters in extreme cases. The position, size, and shape of the stomach vary greatly depending on age, filling state, and body position, with significant interindividual differences.

The stomach is divided into the following sections:

• Cardia (Gastric Entrance, Upper Gastric Orifice, Ostium cardiacum):
  The cardia is a 1–2 cm region where the esophagus transitions into the stomach. The sharp junction between the esophageal and gastric mucosa, often visible endoscopically, marks this area
   
• Fundus gastricus (Gastric Fundus):
  Located above the gastric entrance, the fundus arches upward, also known as the gastric dome or Fornix gastricus. It is usually filled with air swallowed involuntarily during eating. In an upright position, the fundus forms the highest point of the stomach, and the collected air appears as a “gastric bubble” in radiographic images. It is separated from the cardia by a distinct fold, the Incisura cardialis
   
• Corpus gastricum (Gastric Body):
  The main part of the stomach, the corpus, features deep longitudinal mucosal folds (Plicae gastricae), extending from the cardia to the pylorus. These folds are also referred to as the “gastric road”
   
•  Pylorus (Pars pylorica, Gastric Pylorus):
  This section begins with the expanded Antrum pyloricum, followed by the pyloric canal (Canalis pyloricus), and ends with the pylorus itself. The pylorus contains the pyloric sphincter (M. sphincter pylori), a thick circular muscle that closes the lower gastric orifice (Ostium pyloricum), allowing periodic passage of chyme into the duodenum

The stomach is intraperitoneal, covered by serosa except for the dorsal cardia. The embryonic mesogastria rotate from a sagittal to a frontal position during development:

• The Omentum minus extends from the lesser curvature to the liver hilum
• The Omentum majus extends from the greater curvature to the transverse colon, spleen, and diaphragm

The stomach is located intraperitoneally, which gives it a serosal covering, except for the posterior portion of the cardia, which lacks serosa. During embryonic development, the mesogastria undergo a rotation from their original sagittal orientation to a frontal position. The omentum minus extends from the lesser curvature to the porta hepatis, while the omentum majus spreads out from the greater curvature to the transverse colon, spleen, and diaphragm.

The stomach is anchored and stabilized within the abdominal cavity by ligaments that extend to the liver and spleen. Its convex side forms the greater curvature (greater gastric curvature/curvatura major), while its concave side creates the lesser curvature (lesser gastric curvature/curvatura minor). The anterior wall is referred to as the paries anterior, and the posterior wall as the paries posterior. The greater curvature gives rise to the omentum majus, and the omentum minus stretches between the left liver lobe and the lesser curvature.

The gastric wall has a characteristic layered structure when viewed microscopically, progressing from the innermost to the outermost layers:

Tunica mucosa (Mucosal Layer):
This layer lines the stomach’s interior and consists of three sublayers:

• Lamina epithelialis mucosae: Produces a thick, neutral mucus that protects the gastric mucosa from mechanical, thermal, and enzymatic damage
• Lamina propria mucosae: Contains the gastric glands (Glandulae gastricae)
• Lamina muscularis mucosae: A thin muscular layer capable of altering the mucosal relief

Tela submucosa (Submucosal Layer):
This loose connective tissue layer provides a sliding surface and contains:

• A dense network of blood and lymphatic vessels
• The Plexus submucosus (Meissner’s plexus): Regulates gastric secretion, functioning autonomously with modulation by the autonomic nervous system

Tunica muscularis (Muscular Layer):
A robust layer subdivided into:

• Fibrae obliquae: Inner oblique muscle fibers
• Stratum circulare: Middle circular muscle layer
• Stratum longitudinale: Outer longitudinal muscle layer

These layers enable gastric peristalsis, mixing chyme with gastric juice. Between the circular and longitudinal layers lies the Plexus myentericus (Auerbach’s plexus), which autonomously regulates muscle function while receiving input from the autonomic nervous system.

Tela subserosa (Subserosal Layer):
A connective tissue layer providing additional structural support.
 

Tunica serosa (Serosal Layer):
The outermost layer consists of:

• Lamina propria serosae: Contains blood vessels, lymphatics, nerves, and immune cells (e.g., Macula lactea or milk spots)
• Lamina epithelialis serosae: A single-layered squamous epithelium providing a slippery surface to reduce friction with adjacent organs

Gastric Glands (Glandulae gastricae):
Gastric glands are located in the Lamina propria mucosae and are particularly abundant in the fundus and corpus. Around 100 glands per mm² are present in the mucosa, composed of different cell types:

• Mucous cells: Produce neutral mucus, identical to the epithelial cells’ secretion
• Neck cells: Located near the gland’s surface; secrete alkaline mucus rich in bicarbonate ions to regulate pH and protect against self-digestion. These cells are abundant in the cardia and fundus
• Chief cells: Produce pepsinogen, an inactive precursor of pepsin, which activates upon contact with hydrochloric acid (HCl) at the gland’s surface. These cells are concentrated in the gastric corpus
• Parietal cells (Belegzellen): Found primarily in the corpus; they produce:
  • Hydrogen ions (H⁺) for HCl synthesis, resulting in a gastric pH of 0.9 – 1.5
• Intrinsic factor: essential for forming a complex with dietary vitamin B12 to enable absorption through the intestinal wall. This factor is critical for erythropoiesis; its absence after gastrectomy may lead to anemia
• G-cells: Predominantly located in the antrum, these cells secrete gastrin, stimulating HCl production in parietal cells

This intricate structure enables the stomach to perform its functions of digestion, mechanical mixing, and protection from its acidic environment.

The stomach acts as a reservoir for ingested food, storing and mixing it. It produces acidic gastric juice (mucus and HCl) and enzymes that begin the digestion of some food components. The resulting chyme is then gradually released into the duodenum through the pylorus in a regulated manner.

The stomach can store food for several hours, allowing for fewer, larger meals to meet daily nutritional needs.

The arterial blood supply to the stomach is derived from branches of the unpaired celiac trunk. These vessels run along the gastric curvatures as vascular arcades, forming numerous anastomoses:

• Arteria gastrica dextra: From the proper hepatic artery, supplying the lower portion of the lesser curvature
• Arteria gastrica sinistra: Supplying the upper portion of the lesser curvature
• Arteriae gastricae breves: From the splenic artery, supplying the fundus
• Arteria gastroepiploica (omentalis) dextra: From the gastroduodenal artery, supplying the lower (right) portion of the greater curvature
• Arteria gastroepiploica (omentalis) sinistra: From the splenic artery, supplying the left portion of the greater curvature
• Arteria gastrica posterior: From the splenic artery, supplying the posterior gastric wall

The stomach is nourished by two major vascular arcades:

• Along the lesser curvature (formed by the left and right gastric arteries)
• Along the greater curvature (formed by the left and right gastroepiploic arteries)

Venous Supply
The venous drainage of the stomach parallels its arterial supply, with four main veins running along the curvatures. These veins drain into collecting veins that ultimately empty into the portal vein:

• V. gastrica sinistra and dextra: Drain directly into the portal vein
• V. gastroomentalis sinistra and Vv. gastricae breves: Drain into the splenic vein
• V. gastroomentalis dextra: Drains into the superior mesenteric vein

Neural Supply
The stomach’s innervation is primarily through the autonomic nervous system, with additional sensory fibers:

• Sympathetic fibers: Regulate the pyloric musculature
• Parasympathetic fibers (N. vagus, cranial nerve X): Innervate the rest of the gastric musculature and glands
• The left vagus nerve (Truncus vagalis anterior) runs to the anterior stomach surface
• The right vagus nerve (Truncus vagalis posterior) runs to the posterior surface
• Both nerves pass through the diaphragm via the esophageal hiatus
• Sensory fibers: Afferent fibers travel through the N. splanchnicus major to thoracic spinal ganglia

The stomach’s draining lymphatic vessels run parallel to its arterial and venous supply:

• Lesser curvature: Lymph drains alongside the left and right gastric arteries (Aa. gastricae sinistra/dextra) to the left and right gastric lymph nodes (Nll. gastrici sinistri/dextri)
• Fundus: Lymph flows parallel to the splenic artery (A. splenica) to the splenic lymph nodes (Nll. splenici)
• Greater curvature: Lymph drains along the greater omentum to the right and left gastroepiploic lymph nodes (Nll. gastroomentales dextri/sinistri)
• Pylorus region: Lymph drains to the pyloric lymph nodes (Nll. pylorici)

From these regional lymph nodes, the lymph flows to the celiac lymph nodes (Nll. coeliaci), the upper mesenteric lymph nodes, and ultimately into the thoracic duct (Ductus thoracicus).

Additionally, lymph can drain into the pancreatic lymph nodes (Nll. pancreatici), enabling gastric tumors to metastasize to the pancreas. A characteristic feature of advanced gastric carcinoma is the presence of a prominent lymph node in the left supraclavicular region (Virchow’s node), indicating metastatic disease.

Lymph Node Compartments for Surgical Consideration

For surgical purposes, gastric lymph node stations are divided into three compartments:

• Compartment I (Lymph Node Groups 1 - 6): Nodes directly adjacent to the stomach:
  • Paracardial nodes: Groups 1 and 2. Nodes along the lesser and greater curvatures: Groups 3 and 4. Supra- and infrapyloric nodes: Groups 5 and 6
• Compartment II (Lymph Node Groups 7 - 11): Nodes along the major vessels:
  • Along A. gastrica sinistra: Group 7. Along A. hepatica communis: Group 8. Around the celiac trunk: Group 9. Splenic hilum nodes: Group 10. Along the splenic artery (A. lienalis): Group 11
• Compartment III (Lymph Node Groups 12 - 16):
  • Nodes located in more distant regions: Along the hepatoduodenal ligament: Group 12. Behind the pancreatic head: Group 13
  • Mesenteric root and mesentery nodes: Groups 14 and 15 Along the abdominal aorta: Group 16

This structured lymph node mapping aids in planning and executing oncological surgeries for gastric cancer.

GERD occurs when the reflux of gastric contents into the esophagus causes esophageal or extraesophageal symptoms, or significantly impairs quality of life. While the pathogenesis of GERD is multifactorial, it primarily results from an insufficient antireflux barrier.

Antireflux Barrier

Due to higher intra-abdominal pressure compared to thoracic pressure—exacerbated by coughing or the Valsalva maneuver—a functional barrier is essential to prevent reflux. The key components of the antireflux barrier include:

• Function and position of the lower esophageal sphincter (LES)
• External compression by diaphragmatic crura
• Acute His angle (50° – 60°) between the distal esophagus and proximal stomach
• Phrenoesophageal ligament

Three main forms of antireflux barrier insufficiency can occur independently or in combination:

• Transient LES relaxation
• Permanently reduced LES pressure
• Altered anatomy (e.g., hiatal hernia or obtuse His angle)

In mild GERD, transient LES relaxations predominate, while severe GERD is often associated with hiatal hernia and/or persistently low LES pressure.

Transient LES Relaxation

In both healthy individuals and GERD patients with normal resting LES pressure (>10 mmHg), reflux can result from transient, non-swallow-induced LES relaxations. Unlike swallow-induced relaxations, transient relaxations are not accompanied by esophageal peristalsis and last longer. The difference between healthy individuals and GERD patients lies in the type of reflux:

• In healthy individuals, transient relaxations mainly result in gas reflux (“belching”)
• In GERD patients, these relaxations cause acid reflux

Triggers for transient relaxations include vagovagal reflexes induced by proximal gastric distension.

Lower esophageal sphincter and Hiatal Hernia

The LES is a 3 – 4 cm segment of smooth muscle with a normal pressure of 10 – 30 mmHg, regulated by calcium-dependent muscular contraction and cholinergic neural control. Reflux occurs when intra-abdominal pressure exceeds LES pressure or when LES pressure is abnormally low (0 – 4 mmHg).

The diaphragmatic crura, approximately 2 cm long, serve as an “external” sphincter during increases in intra-abdominal pressure.Hiatal hernia predisposes to GERD through various mechanisms, including:

• Separation of the LES from the diaphragmatic crura, reducing their combined sphincter function
• Decreased basal LES pressure and increased transient relaxations
• Facilitated acid reflux during swallow-induced LES relaxations

Types of hiatal hernias:

• Axial hiatal hernia (Type I): Most common form
• Paraesophageal hernia (Type II)
• Combined axial and paraesophageal hernia (Type III)
• Complex hiatal hernia (Type IV): This is the most common site for an upside-down stomach (thoracic stomach), which can be further classified into partial and total types. May include other organs (e.g., colon, spleen) in the thorax (Enterothorax)

His Angle

The His angle is the acute angle (50° – 60°) formed between the abdominal esophagus and the gastric fundus, maintained by the phrenoesophageal ligament.

• Pathological changes: Ligament loosening can cause the angle to become obtuse (> 90°), leading to ineffective closure of the LES and subsequent GERD due to cardia insufficiency

Acid, Pepsin, and Bile Acids

Acid and pepsin play a central role in the development of symptoms and esophageal lesions in GERD.

• In GERD, the volume of acid secretion is typically normal, but the defective antireflux barrier allows acid and pepsin to contact the acid-sensitive esophageal mucosa
• Proton pump inhibitors are effective in GERD treatment, highlighting the role of acid.Bile acids exacerbate the damaging effects of acid and pepsin in duodenogastroesophageal reflux (DGOR):
  • Conjugated bile acids cause erosion at acidic pH
  • Unconjugated bile acids increase esophageal mucosal permeability at alkaline pH